The Janux platform enables the rapid identification of TRACTr and TRACIr development candidates due to a modular design that provides multiple opportunities to rapidly develop therapeutics. The Janux pipeline targets multiple solid tumor indications including metastatic castrate-resistant prostate cancer, colorectal cancer, squamous cell carcinoma of the head and neck, triple-negative breast cancer, urothelial cancer, and non-small cell lung cancer.
Each of these tumor targets are clinically validated and implicated in solid tumors with high prevalence. We are also applying our proprietary technology to develop a costimulatory bispecific product candidate against programmed death-ligand 1 (PD-L1) and CD28 designed to further enhance the anti-tumor activity of T cells, which we believe has the potential to be used as a single-agent or in combination with our current TRACTr pipeline.
|WHOLLY OWNED TRACTr PROGRAMS||Targets||Initial Indications||Discovery||IND-Enabling||Phase 1||Phase 2||Phase 3||Anticipated Milestones|
|WHOLLY OWNED TRACTr PROGRAMS|
|JANX007||PSMA x CD3||mCRPC|
|JANX008||EGFR x CD3||CRC, NSCLC, SCCHN|
|TROP2-TRACTr||TROP2 x CD3||TNBC, UC, NSCLC|
|WHOLLY OWNED TRACIr PROGRAMS|
|PD-L1 x CD28||PD-L1 x CD28||Solid Tumors|
PSMA x CD3
EGFR x CD3
TROP2 x CD3
|PD-L1 x CD28|
PD-L1 x CD28
JANX007 is our novel TRACTr therapeutic targeting prostate-specific membrane antigen (PSMA) for the treatment of metastatic castration-resistant prostate cancer (mCPRC).
JANX008 is our novel TRACTr therapeutic targeting epidermal growth factor receptor (EGFR) for the treatment of multiple solid cancers including, metastatic colorectal cancer (mCRC), squamous cell carcinoma of the head and neck (SCCHN), and non-small cell lung cancer (NSCLC).
Our TROP2-TRACTr is an TROP2xCD3 bispecific T cell engager designed to generate potent anti-tumor activity in solid tumor patients.
PD-L1 x CD28
Our PD-L1xCD28 costimulatory bispecific program is designed to amplify existing T cell anti-tumor responses as well as TRACTr activity through a dual mechanism of (i) blocking tumor-expressed immunosuppressive signaling and (ii) activating T cell costimulatory signaling.